MiR-148a inhibits angiogenesis by targeting ERBB3☆

MicroRNAs (miRNAs) play an important role in carcinogenesis in various solid cancers including breast cancer. Down-regulation of microRNA-148a (miR-148a) has been reported in certain cancer types. However, the biological role of miR-148a and its related targets in breast cancer are unknown yet. In t...

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Main Authors: Yu, Jing, Li, Qi, Xu, Qing, Liu, Lingzhi, Jiang, Binghua
Format: Online
Language:English
Published: Editorial Department of Journal of Biomedical Research 2011
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3597061/
id pubmed-3597061
recordtype oai_dc
spelling pubmed-35970612013-04-02 MiR-148a inhibits angiogenesis by targeting ERBB3☆ Yu, Jing Li, Qi Xu, Qing Liu, Lingzhi Jiang, Binghua Research Paper MicroRNAs (miRNAs) play an important role in carcinogenesis in various solid cancers including breast cancer. Down-regulation of microRNA-148a (miR-148a) has been reported in certain cancer types. However, the biological role of miR-148a and its related targets in breast cancer are unknown yet. In this study, we showed that the level of miR-148a was lower in MCF7 cells than that in MCF10A cells. V-erb-b2 erythroblastic leukemia viral oncogene homolog 3 (ERBB3) is a direct target of miR-148a in human breast cancer cells through direct binding of miR-148a to ERBB3 3′-UTR region. Overexpression of miR-148a in MCF7 cells inhibited ERBB3 expression, blocked the downstream pathway activation including activation of AKT, ERK1/2, and p70S6K1, and decreased HIF-1α expression. Furthermore, forced expression of miR-148a attenuated tumor angiogenesis in vivo. Our results identify ERBB3 as a direct target of miR-148a, and provide direct evidence that miR-148a inhibits tumor angiogenesis through ERBB3 and its downstream signaling molecules. This information would be helpful for targeting the miR-148a/ERBB3 pathway for breast cancer prevention and treatment in the future. Editorial Department of Journal of Biomedical Research 2011-05 /pmc/articles/PMC3597061/ /pubmed/23554686 http://dx.doi.org/10.1016/S1674-8301(11)60022-5 Text en © 2011 by the Journal of Biomedical Research. All rights reserved. This work is licensed under a Creative Commons Attribution 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by/3.0/
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Yu, Jing
Li, Qi
Xu, Qing
Liu, Lingzhi
Jiang, Binghua
spellingShingle Yu, Jing
Li, Qi
Xu, Qing
Liu, Lingzhi
Jiang, Binghua
MiR-148a inhibits angiogenesis by targeting ERBB3☆
author_facet Yu, Jing
Li, Qi
Xu, Qing
Liu, Lingzhi
Jiang, Binghua
author_sort Yu, Jing
title MiR-148a inhibits angiogenesis by targeting ERBB3☆
title_short MiR-148a inhibits angiogenesis by targeting ERBB3☆
title_full MiR-148a inhibits angiogenesis by targeting ERBB3☆
title_fullStr MiR-148a inhibits angiogenesis by targeting ERBB3☆
title_full_unstemmed MiR-148a inhibits angiogenesis by targeting ERBB3☆
title_sort mir-148a inhibits angiogenesis by targeting erbb3☆
description MicroRNAs (miRNAs) play an important role in carcinogenesis in various solid cancers including breast cancer. Down-regulation of microRNA-148a (miR-148a) has been reported in certain cancer types. However, the biological role of miR-148a and its related targets in breast cancer are unknown yet. In this study, we showed that the level of miR-148a was lower in MCF7 cells than that in MCF10A cells. V-erb-b2 erythroblastic leukemia viral oncogene homolog 3 (ERBB3) is a direct target of miR-148a in human breast cancer cells through direct binding of miR-148a to ERBB3 3′-UTR region. Overexpression of miR-148a in MCF7 cells inhibited ERBB3 expression, blocked the downstream pathway activation including activation of AKT, ERK1/2, and p70S6K1, and decreased HIF-1α expression. Furthermore, forced expression of miR-148a attenuated tumor angiogenesis in vivo. Our results identify ERBB3 as a direct target of miR-148a, and provide direct evidence that miR-148a inhibits tumor angiogenesis through ERBB3 and its downstream signaling molecules. This information would be helpful for targeting the miR-148a/ERBB3 pathway for breast cancer prevention and treatment in the future.
publisher Editorial Department of Journal of Biomedical Research
publishDate 2011
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3597061/
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